This study aimed to assess the effects of nicotine on spermatogenesis in 140 mature male albino rats divided into group A (controls), group B (sham controls), group C (nicotine treated) and group D (nicotine withdrawal). Group C was subdivided into CI, CII, CIII according to the dose of injected nicotine (0.2, 0.4 and 0.6 mg nicotine per 100 g per day), where each subgroup was further subdivided according to the treatment duration into subgroups a, b and c that received nicotine for 2, 4 and 8 weeks. Group D received nicotine for 8 weeks followed by withdrawal for another 8 weeks to assess testicular recovery. Testicular tissue sections were subjected to haematoxylin and eosin, Masson's trichrome stains and morphometry. The results showed that nicotine caused degenerative changes in the seminiferous tubules, revealed by altered general tubular architecture, decreased thickness of the spermatogenic cell masses, Sertoli cell vacuolation and thickened basal lamina. These changes were proportional to the nicotine dose and duration. Following nicotine withdrawal, regeneration of the damaged seminiferous tubules was observed to be rather complete in CI group. It is concluded that nicotine could adversely affect testicular spermatogenesis in a dose- and time-dependent manner which would be almost reversible after nicotine withdrawal, especially after small doses.

The cervical rib is an extra rib that develops as a result of elongation of the costal element of the transverse mass of the C7 vertebra. Its incidence ranges from less than 0.5 to 2.5 %, with some gender and laterality predilections, in different populations. It is rarely symptomatic. When large, it can cause various vascular and neurological symptoms. Thoracic outlet syndrome (TOS) is a group of manifestations that result from compression of one or more of the neurovascular structures in the thoracic outlet. The causes of TOS include musculoskeletal variations or anomalies, fibrous bands, tumors and post-traumatic conditions. Clinically, three forms of the TOS are identified: arterial, venous and neurogenic. Surgical options for decompression of the TOS include the transaxillary, the supraclavicular and the posterior subscapular approaches.

Teratology is the science that investigates the congenital malformations and their causes. Intrauterine exposure to a toxicant, particularly in early pregnancy, induces embryonic and fetal changes ranging from none up to malformations and stillbirths. The teratogenic agents include some viral, spirochetal and protozoal infections, physical agents as ionizing radiations and excessive heat, pharmacological drugs as thalidomide, excessive vitamin A, corticosteroids, antiepileptic, antimalarial, antileishmaniasis and antihypertensive agents, industrial pollutants as toluene and cadmium, alcohol and smoking abuse, and narcotics. Maternal health problems as diabetes mellitus, multiple sclerosis and rheumatoid arthritis may also add to the etiology list of teratogenesis. The prevalence of the congenital birth defects ranges from 2 to 5% throughout the first year of postnatal life.

Aging is an inevitable, progressive and irreversible process that is manifested with multiple organ dysfunction. Reactive oxygen species (ROS) is considered the main etiological factor of aging. The thymus gland is the primary site of T cell production and it represents a key organ of the immune system. It is endodermal in origin and lies in the anterior mediastinum behind the sternum. Thymic involution with aging results in less efficient T-cell development and decreased emigration of naïve T cells to the periphery. Deterioration of the immune system with aging contributes to increased incidence of infection, autoimmunity, and cancer, thus increasing the rates of morbidity and mortality in elderly humans.

Intrauterine growth restriction (IUGR) is considered the most common cause of low birth weight or small for gestational age (SGA) birth. When the maternal environment during pregnancy is perturbed, from events such as hypoxia, stress, toxins, inflammation, and placental hypo perfusion, impaired fetal development will result. The main underlying mechanism of IUGR is chronic placental insufficiency that interrupts oxygen and nutrients supply to the fetus resulting in an abnormal fetal growth; the placenta shows functional and structural changes. IUGR is either symmetrical or asymmetrical. It is a major cause of perinatal morbidity and mortality. The condition is frequently associated with neurodevelopment, metabolic and cardiovascular impairments early in infancy and late in adulthood.